23 research outputs found

    H2S biosynthesis and catabolism: new insights from molecular studies

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    Hydrogen sulfide (H2S) has profound biological effects within living organisms and is now increasingly being considered alongside other gaseous signalling molecules, such as nitric oxide (NO) and carbon monoxide (CO). Conventional use of pharmacological and molecular approaches has spawned a rapidly growing research field that has identified H2S as playing a functional role in cell-signalling and post-translational modifications. Recently, a number of laboratories have reported the use of siRNA methodologies and genetic mouse models to mimic the loss of function of genes involved in the biosynthesis and degradation of H2S within tissues. Studies utilising these systems are revealing new insights into the biology of H2S within the cardiovascular system, inflammatory disease, and in cell signalling. In light of this work, the current review will describe recent advances in H2S research made possible by the use of molecular approaches and genetic mouse models with perturbed capacities to generate or detoxify physiological levels of H2S gas within tissue

    Do lifestyle or social factors explain ethnic/racial inequalities in breast cancer survival?

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    Despite numerous studies documenting ethnic inequalities in breast cancer survival between minority and majority ethnic groups worldwide, reasons for these inequalities remain unclear. The authors performed a systematic review of published literature to identify studies that investigated the explanatory power of smoking, alcohol consumption, body mass index (BMI), and socioeconomic position (SEP) on ethnic inequalities in breast cancer survival. Sixteen studies were included in the review. From 5 studies, the authors found that differences in breast cancer survival between ethnic groups may be in part explained by BMI, but there was little evidence to implicate smoking or alcohol consumption as explanatory factors of this inequality. From 12 studies, the authors found that SEP explains part of the ethnic inequality in all-cause survival but that it was not evident for breast-cancer-specific survival. SEP explains more of the disparities among African-American versus white women in the United States compared with other ethnic comparisons. Furthermore, given social patterning of BMI and other lifestyle habits, it is possible that results for SEP and BMI are measuring the same effect. In this review, the authors make suggestions regarding the role of epidemiology in facilitating further research to better inform the development of effective policies to address ethnic differences in survival

    Maternal adiposity—a determinant of perinatal and offspring outcomes?

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    Experimental and animal data suggest that maternal obesity during pregnancy adversely affects offspring health in the short-term and the long-term. Whether these effects occur in humans and influence population health is less clear. This Review explores evidence from intervention studies and observational studies that have used designs (such as family-based comparisons and Mendelian randomization) that might help improve understanding of the causal effects of maternal obesity in humans. Collectively, human studies provide evidence that maternal overweight and obesity is causally related to pregnancy complications, increased offspring weight and adiposity at birth, and the difficulties associated with delivery of large-for-gestational-age infants. The underlying mechanisms for these effects probably involve maternal and fetal dysregulation of glucose, insulin, lipid and amino acid metabolism. Some evidence exists that extreme maternal obesity (BMI ≥40 kg/m2) is causally related to a long-term increase in offspring adiposity, but further exploration of this relationship is needed. High gestational weight gain may result in a long-term increase in offspring adiposity if women are already overweight or have obesity at the start of pregnancy. To date, little high-quality human evidence exists that any of these effects are mediated by epigenetic mechanisms, but approaches to appropriately test this possibility are being developed
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